Jove
Visualize
联系我们
JoVE
x logofacebook logolinkedin logoyoutube logo
关于 JoVE
概览领导团队博客JoVE 帮助中心
作者
出版流程编辑委员会范围与政策同行评审常见问题投稿
图书馆员
用户评价订阅访问资源图书馆顾问委员会常见问题
研究
JoVE JournalMethods CollectionsJoVE Encyclopedia of Experiments存档
教育
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab Manual教师资源中心教师网站
使用条款与条件
隐私政策
政策

相关概念视频

Epigenetic Regulation01:37

Epigenetic Regulation

3.6K
Epigenetic changes alter the physical structure of the DNA without changing the genetic sequence and often regulate whether genes are turned on or off. This regulation ensures that each cell produces only proteins necessary for its function. For example, proteins that promote bone growth are not produced in muscle cells. Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
X-chromosome...
3.6K
Epigenetic Regulation01:46

Epigenetic Regulation

33.3K
Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
33.3K
Negative Regulator Molecules01:23

Negative Regulator Molecules

38.1K
Positive regulators allow a cell to advance through cell cycle checkpoints. Negative regulators have an equally important role as they terminate a cell’s progression through the cell cycle—or pause it—until the cell meets specific criteria.
38.1K
Replicative Cell Senescence02:15

Replicative Cell Senescence

4.2K
Replicative cell senescence is a property of cells that allows them to divide a finite number of times throughout the organism's lifespan while preventing excessive proliferation. Replicative senescence is associated with the gradual loss of the telomere — short, repetitive DNA sequences found at the end of the chromosomes. Telomeres are bound by a group of proteins to form a protective cap on the ends of chromosomes. Embryonic stem cells express telomerase — an enzyme that adds...
4.2K
Abnormal Proliferation02:23

Abnormal Proliferation

5.0K
Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
5.0K
Maintenance of the ES Cell State01:14

Maintenance of the ES Cell State

2.6K
The cells of the blastocyst inner cell mass only remain pluripotent for a short time. This state of pluripotency and self-renewal can be maintained in embryonic stem (ES) cell culture by adding specific chemicals or growth factors to ensure the cells can continue dividing and later differentiate into different cell types. In some cases, the cells are grown on a feeder layer of differentiated cells, which provides the growth factors and extracellular matrix components necessary for stem cell...
2.6K

您也可能阅读

相关文章

通过共同作者、期刊和引用图与本文相关的文章。

排序
Same author

Targeting the chromatin remodeler BAZ2B mitigates hepatic senescence and MASH fibrosis.

Nature aging·2025
Same author

Identification of a Novel Glycosyltransferase Prognostic Signature in Hepatocellular Carcinoma Based on LASSO Algorithm.

Frontiers in genetics·2022
Same author

Multistimuli-Responsive Squaraine Dyad Exhibiting Concentration-Controlled Vapochromic Luminescence.

ACS applied materials & interfaces·2022
Same author

Fabrication of 3D GelMA Scaffolds Using Agarose Microgel Embedded Printing.

Micromachines·2022
Same author

Reclassification of <i>Enterobacter</i> sp. FY-07 as <i>Kosakonia oryzendophytica</i> FY-07 and Its Potential to Promote Plant Growth.

Microorganisms·2022
Same author

Three-Dimensional Microfilament Printing of a Decellularized Extracellular Matrix (dECM) Bioink Using a Microgel Printing Bath for Nerve Graft Fabrication and the Effectiveness of dECM Graft Combined with a Polycaprolactone Conduit.

ACS applied bio materials·2022

相关实验视频

Updated: Dec 27, 2025

Quantifying Tissue-Specific Proteostatic Decline in Caenorhabditis elegans
09:18

Quantifying Tissue-Specific Proteostatic Decline in Caenorhabditis elegans

Published on: September 7, 2021

3.2K

两种保存的表观遗传调节剂可以防止健康的衰老

Jie Yuan1,2, Si-Yuan Chang1,2, Shi-Gang Yin3,2,4

  • 1Institute of Neuroscience and State Key Laboratory of Neuroscience, CAS Center for Excellence in Brain Science and Intelligence Technology, Chinese Academy of Sciences, Shanghai, China.

Nature
|February 28, 2020
PubMed
概括

科学家发现了一种表观遗传机制, 这涉及到特定的基因,当改变时,可以防止与年龄相关的衰退,并改善模型生物的健康寿命.

更多相关视频

Techniques to Induce and Quantify Cellular Senescence
06:51

Techniques to Induce and Quantify Cellular Senescence

Published on: May 1, 2017

34.7K
A Quantitative Measurement of Reactive Oxygen Species and Senescence-associated Secretory Phenotype in Normal Human Fibroblasts During Oncogene-induced Senescence
13:59

A Quantitative Measurement of Reactive Oxygen Species and Senescence-associated Secretory Phenotype in Normal Human Fibroblasts During Oncogene-induced Senescence

Published on: August 12, 2018

8.5K

相关实验视频

Last Updated: Dec 27, 2025

Quantifying Tissue-Specific Proteostatic Decline in Caenorhabditis elegans
09:18

Quantifying Tissue-Specific Proteostatic Decline in Caenorhabditis elegans

Published on: September 7, 2021

3.2K
Techniques to Induce and Quantify Cellular Senescence
06:51

Techniques to Induce and Quantify Cellular Senescence

Published on: May 1, 2017

34.7K
A Quantitative Measurement of Reactive Oxygen Species and Senescence-associated Secretory Phenotype in Normal Human Fibroblasts During Oncogene-induced Senescence
13:59

A Quantitative Measurement of Reactive Oxygen Species and Senescence-associated Secretory Phenotype in Normal Human Fibroblasts During Oncogene-induced Senescence

Published on: August 12, 2018

8.5K

科学领域:

  • 表观遗传学与衰老
  • 神经科学
  • 遗传学

背景情况:

  • 全球预期寿命有所增加,但健康状况并没有相应改善.
  • 了解健康衰老的生物基础至关重要.
  • 可以将寿命与健康区分开来,强调研究健康衰老机制的需要.

研究的目的:

  • 确定调节健康衰老的表观遗传机制.
  • 研究调节与年龄相关的行为恶化基因.
  • 探索促进健康衰老的潜在治疗目标.

主要方法:

  • 在*Caenorhabditis elegans*中进行全基因组RNA干扰 (RNAi) 查,以确定影响与年龄相关的行为衰退的基因.
  • 研究了C. elegans*中的特定表观遗传调节剂 (BAZ-2和SET-6) 的作用.
  • 在培养的小鼠神经元和人类细胞中验证了发现,并检查了人类数据库和小鼠模型.

主要成果:

  • 在C. elegans*中发现了59个调节与年龄相关的行为恶化基因.
  • 发现神经元表观遗传调节剂BAZ-2和SET-6通过损害线粒体功能加速衰老.
  • 表明人类的正确基因 (BAZ2B,EHMT1) 随着年龄的增长与阿尔茨海默病的进展相关; *Baz2b* 切除可防止小鼠的认知能力下降和不健康的体重增加.

结论:

  • 一个涉及BAZ-2和SET-6的保存表观遗传机制负面调节健康的衰老.
  • 这些表观遗传调节剂影响线粒体功能,并与与年龄相关的认知衰退有关.
  • 这些研究结果表明,促进健康老龄化和延长健康寿命的干预措施可能是目标.